Guidance on Recognising and Managing Medical Emergencies ...

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Guidance on Recognising and Managing Medical Emergencies in Eating Disorders (Replacing MARSIPAN and Junior MARSIPAN)

Annexe 2 : Type 1 diabetes and eating disorders (T1DE) Draft for Stakeholder review – July 2021

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Editors

Simon Chapman, Consultant Paediatrician, King’s College Hospital and South

London and the Maudsley NHS Foundation Trusts

Helen Partridge, University Hospitals Dorset NHS Foundation Trust

Claire Pinder, Eating Disorders Dietitian, Dorset HealthCare University NHS

Foundation Trust

Marietta Stadler, King’s College Hospital NHS Foundation Trust

Writing group, list of contributors

Sarah Alicea, Children and Young People's Diabetes Specialist Dietitian, University

Hospitals Dorset NHS Foundation Trust

Michelle Bennett, Clinical Specialist in Eating Disorders, Dorset HealthCare University

NHS Foundation Trust

Dr Sarah Brewster, Diabetes and Endocrinology Registrar/Clinical Academic Fellow,

Southern Health NHS Foundation Trust

Caroline Cross, ComPASSION Project Manager, Dorset HealthCare University NHS

Foundation Trust

Dr Carla Figueiredo, Consultant Psychiatrist; Dorset HealthCare University NHS

Foundation Trust

Linda Gerrard-Longworth, Eating Disorders Therapist, Southern Health NHS

Foundation Trust

Kerri Hampton, Diabetes Nurse Specialist, Dorset County Hospital NHS Foundation

Trust

Dr Eveleigh Nicholson, Consultant in Diabetes and Endocrinology, Portsmouth

Hospitals University NHS Trust

Dr Helen Partridge, Consultant in Diabetes, University Hospitals Dorset NHS

Foundation Trust

Simone Penfold, Diabetes Specialist Nurse, University Hospitals Dorset NHS

Foundation Trust

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Claire Pinder, Eating Disorders Dietitian, Dorset HealthCare University NHS

Foundation Trust

Dr Lindsey Rouse, Clinical Psychologist, University Hospitals Dorset NHS Foundation

Trust

Jacqueline Ryder, Diabetes Specialist Nurse, University Hospitals Dorset NHS

Foundation Trust

Nicola Stacey, Diabetes Specialist Nurse, University Hospitals Dorset NHS Foundation

Trust

Ariella Thompson, PhD Student, Bournemouth University

Dr Sebastian Zaidman, Dorset HealthCare University NHS Foundation Trust

Reviewers

Jacqueline Allan, Patient Public Involvement representative; DClinPsych Trainee at

South London and the Maudsley Hospitals NHS Foundation Trust

Andrea Brown, Consultant Psychiatrist, Schoen Clinic, London

Helen Cope, Liaison Psychiatrist, Guy’s and St Thomas NHS Foundation Trust

Sophie Harris, Consultant Diabetologist, King’s College Hospital NHS Foundation

Trust

Khalida Ismail, Professor of Psychiatry, King’s College London

Dulmini Kariyawasam, Consultant Diabetologist, Guy’s and St Thomas NHS

Foundation Trust

Yuk-Fun Liu, Consultant Diabetologist, Guy’s and St Thomas NHS Foundation Trust

Ruth Marshall, Child and Adolescent Psychiatrist, Central Manchester CAMHS

Annexe 2: Type 1 diabetes and eating disorders (T1DE)

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Contents

Introduction ....................................................................................................................................... 3

Table 1: Risk assessment table for T1DE .................................................................................. 9

Additional notes to support Table 1: Risk assessment table for T1DE .........................16

Appendices ..................................................................................................................................... 44

Appendix A: Example re-insulinisation and refeeding protocol for people with type 1 diabetes and disordered eating ................................................................................................................ 44

Appendix B: Inpatient protocols for the management of hyperglycaemia and ketones and the management of hypoglycaemia in adults ................................................... 52

Appendix C: Inpatient protocols for the management of refusal of short- and long-acting insulin in adults ..................................................................................................................................... 53

Appendix D: Inpatient insulin management care plan for adults with type 1 diabetes and eating disorders..................................................................................................................... 55

References ....................................................................................................................................... 58

Abbreviations .................................................................................................................................. 62


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Introduction

Interaction between elements of living with type 1 diabetes and the biological,

psychological and social predisposing factors to developing an eating disorder can

precipitate the development of an eating disorder in the context of type 1 diabetes(1).

Type 1 diabetes and disordered eating (T1DE) refers to a range of presentations in

those with a diagnosis of type 1 diabetes that use one or more of a range of

behaviours to control their weight. These include omission or restriction of insulin,

restriction of food, over-exercise, self-induced vomiting, and laxative or diuretic

misuse. Thyroid hormones or diabetes medication believed to reduce body weight

may also be used. Insulin over-injection, either to cover binge eating, or out of fear

that high blood glucose levels may cause long-term complications, have been

observed. Insulin restriction puts patients at higher risk of the short- and long-term

complications of diabetes; insulin over-injection bears the risk of severe

hypoglycaemia and loss of awareness of hypoglycaemia. Studies report that insulin

restriction is associated with a threefold increase in mortality(2) and a reduced

quality of life compared to those with type 1 diabetes who do not restrict insulin(3, 4).

There has yet to be an agreed consensus on how best to define this patient group.

Diagnostic criteria are proposed (Box 1). Most patients are of a normal weight, with a

body mass index (BMI) of 18.5–25 kg/m2 in adults, or above 85% mBMI for children and

young people under the age of 18 years (this would need to be adjusted in Black and

Asian populations). While some patients omit insulin, others restrict their dietary

intake of carbohydrates but use insulin appropriately. As a result, BMI/%mBMI and

HbA1c cannot be used exclusively in the identification or diagnosis of patients with

T1DE. It is also important to recognise that other diabetes-related factors (such as

diabetes distress, depression, anxiety, needle phobia, acceptance of diabetes

diagnosis, fear of complications, fear of hypoglycaemia, or fear of hyperglycaemia)

may lead to diabetes-related behaviours that can be mistaken for T1DE. This is

because presentation may include indicators associated with T1DE, such as raised

HbA1c, weight loss and disengagement from services. A careful history is therefore

required to identify if weight and shape concerns are part of the psychopathology, to

make a differential diagnosis and ensure an appropriate treatment pathway.


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People with T1DE can be fearful of judgement by healthcare professionals, family and

friends and can experience considerable shame and guilt. Sometimes this can be

routed in past adverse experience with health care delivery related to their

diabetes(5). This cohort of patients may therefore disguise the difficulties they are

experiencing or disengage with services or health care professionals. As a result, T1DE

can be easily overlooked. It is recommended that staff in a range of health care

settings including diabetes clinics, ophthalmology, primary care, A&E, acute medical

units, medical and paediatric wards, intensive care units, dental clinics and liaison

psychiatry services are alert to the potential red flags for T1DE (Box 2) and feel

confident to initiate a supportive, non-judgemental conversation with the person, or

in the case of children and young people also with their parents or teachers to

explore the possibility of T1DE being present. Further consideration of the

identification and engagement of this cohort are discussed elsewhere.

Where there is concern it is important to recognise that this cohort require ongoing

treatment. Staff identifying someone at risk of T1DE should therefore refer to

psychiatric liaison or make links with local eating disorder, mental health or diabetes

teams to discuss their concerns.

Box 1: Proposed diagnostic criteria for T1DE

People with type 1 diabetes who present with all 3 criteria:

1. Intense fear of gaining weight, or body image concerns, or fear of

insulin promoting weight gain.

2. Recurrent inappropriate direct or indirect* restriction of Insulin

(and/or other compensatory behaviour**) to prevent weight gain.

3. Person must present with a degree of insulin restriction, eating or

compensatory behaviours that cause at least one of the following:

• harm to health

• clinically significant diabetes distress

• impairment on daily functioning.

* Indirect restriction of insulin refers to reduced insulin need/use due to significant carbohydrate restriction.


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Box 2: Red flags for T1DE

Any one of the following:

Biochemical

• increase in HbA1c above 86 mmol/mol or erratic blood glucose

levels (e.g. high glycaemic variability, post prandial

hyperglycaemia following bolus omission)

• multiple emergency department or ward admissions with

hyperglycaemia, DKA

• recurrent ketonaemia (>3 mmol/L) – may have compensated

metabolic acidosis

• recurrent severe hypoglycaemia (two or more episodes over

24 months)

Beliefs, behaviours and functioning

• over-exercising

• impaired awareness of hypoglycaemia

• extreme dietary restriction or binge eating

• weight loss history (weight loss in line with MaRSiPAN criteria)

or fear of weight gain

• body image concerns

• history of eating disorder diagnosis

• diabetes distress

• fear of hypoglycaemia

• mental health comorbidity (e.g. depression, generalised anxiety

disorder)

Relationships

• secrecy about diabetes management, failure to request regular

prescriptions, disengagement from diabetes services

• poor school/work performance/attendance


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Several factors will have historically resulted in the exclusion of this cohort from the

support and expert treatment that they require. Both eating disorders and type 1

diabetes are specialist areas of medical and psychological expertise. Where T1DE is

suspected or identified, it is essential that expertise is drawn from both specialities to

inform the treatment offered. Good practice would recommend a shared-care model

that provides continuity of care and a unified team approach with joint care plans(6).

Case discussion, professional shadowing, peer-to-peer learning, joint appointments

(face-to-face or virtual), development of referral routes, shared treatment pathways,

case conferences involving the service user, multidisciplinary team meetings and

peer supervision all have the potential to inform improved care.

In acute hospital settings input in adults from the diabetes team alongside the

treating physician is recommended or, in children and young people, by the

paediatric diabetes team, as well as referral to psychiatric liaison within reach from

local eating disorder services as needed:

Registered mental health nurse (RMN); to support nursing care plan including

the management of compensatory behaviours including appropriate

management of insulin administration, advice on level of observations,

requirement for one-to-one support and appropriate restraint procedures.

RMN/mental health support worker; to provide one-to-one support and

appropriate restraint if required.

Eating disorders dietitian; liaison with the treating dietitians regarding the

dietetic care plan.

Consultant psychiatrist; liaison with the treating medical or paediatric team,

advice regarding assessment of capacity, Mental Health Act assessment and

advice on level of observations. If any degree of restraint is required, this would

need to be discussed and advice given around the appropriate legal

safeguards.

In specialist eating disorder units care should be supported by the local diabetes

team. Physical health assessment and medical stabilisation (if indicated: e.g. severe

electrolyte disturbance, metabolic acidosis, dehydration) should be achieved prior to

admission to the eating disorder unit in an acute medical setting:

Adult or paediatric diabetes consultant:

o advice on the insulin management plan and the safe management of

hyperglycaemia, hypoglycaemia and ketones


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o advice on modified rehydration/ re-insulinisation protocols for not too

rapid improvement of glycaemia to avoid too rapid weight gain and

acute neuropathic complications.

Adult or paediatric diabetes specialist nurse:

o to support the RMNs with the implementation of the advised insulin

plan and practical aspects of diabetes management

o Initiating additional physical health investigations (bone health,

endocrine disorders, autonomic neuropathy assessment) as

appropriate.

The assessment of risk in people with T1DE will mirror those with other eating

disorder presentations with some additional considerations. Table 1 shows the

parameters, risks and links to relevant places in this document, including those that

mirror more general eating disorder presentations that have been described in the

main guidance document. See Table 2 for strategies for insulin omission reduction.

General principles for assessment and treatment of this patient group are discussed,

which can be adapted to a range of healthcare settings including primary care,

outpatient diabetes and eating disorder services, acute inpatient settings and

specialist eating disorder units (SEDUs). Additionally, clinicians should check that

annual diabetes review checks are up to date, to include(7–9):

HbA1c measurement

blood pressure measurement

smoking status

weight and BMI measurements, including %mBMI in those under 18 years

albumin: creatinine ratio

full lipid profile (including high-density lipoprotein and low-density lipoprotein,

cholesterol and triglycerides)

electrolytes, estimated glomerular filtration rate (or measured glomerular

filtration rate if extremely underweight)

thyroid hormone status

liver enzymes

electrocardiogram

retinopathy screening


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foot health check.

Consider screening for cortisol deficiency and growth hormone deficiency

(e.g. in case of problematic hypoglycaemia)

Consider screening for coeliac disease (e.g. if underweight, or gastrointestinal

symptoms)

Pre-pregnancy counselling/ contraception counselling.


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Table 1: Risk assessment table for T1DE Parameter Risks Relevant links

within this document

BMI/starvation

(e.g. temperature,

SUSS Test)

As for those in main Guidance on Recognising and Managing Medical Emergencies in

Eating Disorders (replacing MaRSiPAN/Jr MaRSiPAN)

[Note: Links are to be added]

Additional considerations for all levels of risk:

Most T1DE patients fall within the low or moderate risk for BMI. This should not

mask clinician concern because severity of overall risk lies in the consequences of

insulin omission.

Section 2.4

Cellular starvation will be present in the omission of insulin regardless of BMI. Section 2.4

Those with diabetes and cardiac autonomic dysfunction may have a resting

tachycardia, which may mask severity of starvation.

Section 2.4

Insulin administration is the driver for refeeding syndrome in T1DE. Section 2.6

Considerations for insulin during nasogastric tube feeding in T1DE. Appendix A: Example reinsulinisation and refeeding protocol…

Cardiovascular

health/ECG

As for those in main Guidance

Additional considerations at all levels of risk:

Assessment of long-term macrovascular complications of type 1 diabetes should

form part of medical assessment in T1DE. Section 2.12


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Hydration and oedema



Insulin restriction/omission increases risk of dehydration as a result of

hyperglycaemia/ketones.

Section 2.6

Assessment of hydration status should therefore form part of the medical assessment

in T1DE.

Reinsulinisation can be associated with oedema Section 2.11

Biochemical

Hyperglycaemia and raised ketones will occur with reduction or omission of insulin. Appendix B: Inpatient protocols for the management of hyperglycaemia… Section 2.11

Low risk = normal glycaemia.

Moderate risk = hyperglycaemia with ketones absent or recurrent episodes of ketones

< 1.5.

High risk = hyperglycaemia with recurrent episodes of ketones >1.5

Very high risk = 1 or more episodes of DKA associated with deliberate insulin omission

Hypoglycaemia may occur with carbohydrate restriction or excessive exercise

alongside insulin administration.

Appendix B: Inpatient protocols for the management of hyperglycaemia... Section 2.3

Low risk = infrequent episodes requiring self-management of hypoglycaemia.

Moderate risk = frequent episodes requiring self-management of hypoglycaemia

High risk = Infrequent episodes of hypoglycaemia requiring external assistance for

treatment.

Very high risk = severe and recurrent episodes of hypoglycaemia requiring external

assistance for treatment.


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Electrolyte disturbance; as for those in main Guidance


Assessment of renal function as a long-term complication of type 1 diabetes should

form part of the medical assessment in T1DE.

Consider the potential for renal impairment to impact on the biochemical picture.

When considering renal function consider that urea will be reduced in the presence of

starvation.

Acid-base balance; as for those in main Guidance

Insulin omission may further complicate the metabolic picture. Section 2.5

Medication Additional considerations at all levels of risk:

Adjunctive therapies; GLP-1 agonists and SGLT-2 inhibitors should be used with

caution in those with T1DE due the associated weight loss and potential risks of

hypoglycaemia and DKA with SGLT-2 inhibitors.

Section 2.2

Glucagon – will be less effective in the management of hypoglycaemia where

glycogen stores are reduced due to insulin omission, carbohydrate restriction or

excessive exercise.

Section 2.3


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Disordered eating behaviours

Food restriction in the presence of appropriate insulin administration; as for main Guidance


If food restriction is present in the absence or restriction of insulin the risks will be

increased beyond those in main Guidance as availability of calories to the body will be

further reduced.

Section 2.4

Assessment for the presence of gastroparesis as a long-term complication of type 1

diabetes should form part of the medical assessment in T1DE.

Section 2.12

High risk

Be aware of the potential for preferential avoidance of carbohydrate which if insulin is

not adjusted increases the risk of hypoglycaemia.

Section 2.5

Be aware of the potential for the over consumption of carbohydrate, in the absence or

restriction of insulin, to maintain raised blood glucose and ketone levels.

Section 2.5

Bingeing may result in raised blood glucose and ketone levels unless insulin is

appropriately adjusted.

Section 2.5

Person may feel guilt and shame after an episode of bingeing and may

overcompensate with a large insulin dose causing hypoglycaemia.

Section 2.3

Be aware of the potential for diabetic gastroparesis to impact on food patterns and

eating disorder symptomology.

Section 2.12

Be aware that the delayed gastric emptying associated with diabetes related

gastroparesis, can result in hypoglycaemia.

Section 2.3

Very high risk

Binging in context of pre-existing gastroparesis may lead to gastric dilatation,

ischaemia and rupture. Section 2.12


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Activity and

exercise



Increased risk of hypoglycaemia unless carbohydrate and/or insulin are adjusted. Section 2.3

Increased risk of ketosis in those omitting or restricting insulin. Section 2.5

Further impact on hydration and subsequent risk of DKA in those omitting or

restricting insulin

Section 2.1

Impact on foot health. Assessment of foot health should form part of the medical

assessment in T1DE.

Section 2.5

Compensatory

behaviours

As for those in main Guidance All points link to Section 2.5

Additional considerations at all levels of risk: Table 2: Strategies for insulin omission/reduction… Appendix C: Inpatient protocols for the management of refusal of… insulin… Appendix D: Inpatient insulin management care plan…

Strategies to disguise insulin omission/reduction.

Overconsumption of carbohydrate, and exercise in the absence or restriction of insulin

can be used to maintain raised blood glucose and ketone levels.

Emergence of other eating disorder behaviours as T1DE related compensatory

behaviours are addressed.

Vomiting resulting in unpredictable blood glucose levels, further complicated by

insulin omission or restriction if this is present.


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Engagement

with

management

plan

Low risk = has insight/motivation to engage in insulin management plan.

Moderate risk = some insight/motivation to engage in insulin management plan.

High risk = poor insight/motivation to engage in insulin management plan. Sections 1.3 and 4.1

Very high risk = active refusal to engage in/sabotage of insulin management plan. Sections 2.1, 2.42 and

3.6


Be aware that previous negative experiences with health care professionals can impact

on engagement.

Section 3.3

Hyperglycaemia and ketones as well as recurrent hypoglycaemia can impair cognition

and impact the ability to engage in treatment plans.

Sections 4.4, 4.6 and

4.7

Be aware of the potential for diabetes related psychological concerns to impact on

treatment progression.

Section 4.2

Be aware that lack of insight can impact on engagement with treatment.

Be aware that family dynamics can impact on treatment progression.

Other mental

health

diagnoses



Increased risk of depression and anxiety in those with type 1 diabetes compared to the

general population.

All points link to

Section 3.3

Consider other diabetes related aspects of mental health including diabetes related

distress, needle phobia, fear of hypoglycaemia, fear of diabetes related complications.


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Self-harm and

suicide



Suicide occurs more frequently with the coexistence of psychiatric and physical

illness.

Be aware of insulin as an available and lethal means of harm. All points link to Section 3.4

Use of the

Mental Health

Act



Use of the Mental Health Act in physical illness. Section 3.8

Annual diabetes

review checks


weight and body mass index measurements

blood pressure measurement

smoking status

HbA1c measurement

albumin: creatinine ratio

full lipid profile (including high-density and low-density lipoproteins, cholesterol and

triglycerides)

retinopathy screening

foot check.


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Additional notes to support Table 1:

Risk assessment table for T1DE

Body mass index and starvation

Risks associated with low BMI/%mBMI and starvation in T1DE will mirror those

without type 1 diabetes. It should be noted that those with diabetes and cardiac

autonomic dysfunction, or significant dehydration due to glucosuria/ polyuria may

have a resting tachycardia which would invalidate heart rate as an indicator for

severity of starvation. This is less likely to be a phenomenon seen in children and

young people.

Most people with a diagnosis of T1DE fall within low or moderate risk for BMI/%mBMI.

However, it is important that this does not mask clinician concern because it is

important to recognise that the most acute risks result from metabolic sequelae

associated with omission of insulin, where this is present, because these can occur at

any weight (see Biochemical risks in this annexe).

Refeeding/re-insulinisation

Cellular starvation of insulin dependent tissue that is caused by insulin deficiency will

occur regardless of weight, BMI or the other markers of starvation. In patients with

T1DE, where insulin has been omitted and/or carbohydrate restricted, the

reintroduction of insulin alongside carbohydrate will be the key driver for the

refeeding syndrome. All those with insulin omission are potentially at risk of

electrolyte shifts on re-insulinisation/refeeding. Re-insulinisation is the process of

insulin reintroduction, while refeeding describes the reintroduction of food,

particularly carbohydrates. Theory would suggest that the degree of risk will be

associated with the severity of insulin omission and the rate of insulin reintroduction.

Low initial electrolytes, vomiting, laxative, alcohol or drug misuse and infection all

increase the risk of refeeding syndrome further in those without type 1 diabetes(10)

and should be considered in this patient cohort. In children and young people, risks

include hypophosphataemia before re-alimentation, core temperature below 36

degrees Celsius and low %mBMI(11). Electrolyte shifts (e.g. hypokalaemia or

hyponatraemia) will be more pronounced in a person with diabetes than in a person


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without diabetes, therefore electrolytes have to be monitored closely, with

appropriate medical/diabetes/paediatric oversight.

In those with T1DE, who have been omitting insulin, the risk of re-

insulinisation/refeeding syndrome can be managed by a gradual introduction of

insulin (and carbohydrate if this has been restricted). There are other reasons for a

gradual approach which if ignored all have the potential to deter the person with

T1DE continuing with treatment:

Building up insulin and food slowly gives time to address psychological

concerns associated with this process. Some T1DE service users will find rapid

increases in the carbohydrate content of their meal plan distressing. It is

important that the patient is able to engage with the meal plan and a daily

carbohydrate intake (distributed over three main meals and snacks, excluding

hypoglycaemia treatment) of approximately 150 g of carbohydrates as a

starting point is deemed to be safe, and can be modified on a case-by-case

basis.

It will reduce the risk of insulin-/refeeding-related oedema which although

usually medically harmless can have a psychological impact as a result of rapid

weight changes.

It will allow adjustment to post-meal feelings of fullness which can be

interpreted as ‘being fat’. This can be as a result of delayed gastric emptying

which can occur if food restriction has been present or if diabetes-related

gastroparesis is present. Another driver for delayed gastric emptying is

hyperglycaemia per se, therefore investigations for gastroparesis should be

conducted once stabile normoglycaemia has been safely achieved.

A gradual reduction in blood glucose levels will reduce the risk of

complications, i.e. treatment induced retinopathy and neuritis(12, 13) (see

Biochemical risks in this annexe).

It will reduce the risk of hypoglycaemia or the frequency of pseudo

hypoglycaemia (see Biochemical risks in this annexe).

Counselling of the T1DE service user on all the above (in particular about the

transient nature of the oedema-/fluid retention-related weight gain and about

the rationale for a slow titration process) is important at all stages of this

process.

While a gradual approach is advocated, this needs to be balanced against the risks of

diabetic ketoacidosis (DKA) (see Biochemical risks in this annexe) and underfeeding.


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Any protocol needs to ensure enough insulin is initially provided to ensure ketone

production is switched off. The aim should then be initial conservative glucose

targets while gradually increasing insulin and food (including carbohydrate) to

achieve weight stabilisation or weight gain (if required) and prevent ongoing

physical deterioration. The requirement for certain vitamins, in particular thiamine

and other B vitamins during the refeeding process can be assumed to mirror those

without type 1 diabetes.

An example protocol for re-insulinisation/oral refeeding in T1DE that has so far been

found to be safe and acceptable to service users can be found in Appendix A. Where

re-insulinisation/refeeding is progressed more rapidly or if other risk factors for the

development of refeeding syndrome are present, such as infection or abnormal

baseline electrolytes, increased frequency of monitoring of electrolytes is advised,

based on clinical judgement and reflecting levels that would be provided to those

without type 1 diabetes as a minimum.

It should be noted that in atypical presentations of T1DE, where insulin is not omitted

and HbA1c is not elevated, carbohydrate reintroduction alongside appropriate doses

of insulin to maintain appropriate blood glucose levels would be advocated. Under

these circumstances the rate of carbohydrate introduction needs to be appropriately

managed to reduce the risk of electrolyte shifts on refeeding. It is suggested that

standard refeeding protocols used for the management of refeeding syndrome in

those who do not have type 1 diabetes would be appropriate to use under these

circumstances, alongside matched insulin doses.

Principles of medical management

There are many factors to consider in the medical management of this patient group

and it is essential to ensure appropriate medical oversight is in place to monitor

electrolyte and fluid imbalances, blood glucose and ketones.

Electrolyte shifts (e.g. hypokalaemia or hyponatraemia) will be more

pronounced in a person with diabetes than in a person without diabetes,

therefore electrolytes have to be monitored closely, with appropriate

medical/diabetes/paediatric oversight.

DKA (see Biochemical risks in this annexe) must be excluded or appropriately

managed prior to the initiation of either conventional refeeding or nasogastric

tube feeding.


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Patients are likely to have significant concerns around both

calorie/carbohydrate intake AND insulin administration with risk of refusal of

either or both. Anxiety levels are therefore likely to be extremely high. In an

acute setting referral to psychiatric liaison is essential and advice sought from

local eating disorder/mental health services in order that appropriate

management plans can be put in place, including sectioning under the Mental

Health Act 1983 (updated 2007) and use of restraint if required (see Use of the

Mental Health Act in this annexe).

Blood glucose and ketone levels are likely to be high initially (a combination of

starvation effect and insulin deficiency); once DKA has been ruled out (or

adequately treated) monitoring of ketones and glucose should be ongoing,

with frequency determined by the clinical situation to ensure an appropriate

and safe reduction. Rapid correction of blood glucose levels can precipitate

acute, unpleasant symptoms of neuropathy (including autonomic neuropathy

and gastroparesis), retinopathy and insulin oedema9,10 (see Biochemical risks in

this annexe).

Patients are likely to experience symptoms of hypoglycaemia at much higher

glucose levels than would be expected. While medical management of

pseudo hypoglycaemia (physical symptoms of hypoglycaemia but at glucose

levels above those accepted as defining hypoglycaemia) is not required it can

be distressing for the patient and a pre-defined quick acting

carbohydrate treatment portion can be offered to treat their symptoms (see

Biochemical risks in this annexe).

The rate of change of glucose should therefore be controlled and it may be

necessary to start at very low insulin infusion rates initially and accept higher

blood glucose levels (see Biochemical risks in this annexe). We have some

experience of using insulin at a total daily dose of 0.2–0.3 units/kg body weight

as an initial oral refeeding/re-insulinisation protocol without significant

detrimental shifts in electrolytes, hypoglycaemia or development of ketosis.

We recommend that decisions around starting dose of insulin are undertaken

with close supervision by a senior member of the diabetes team, dietitian and

physician with clinical responsibility for the patient. A graduated approach to

insulin reintroduction will also help to manage patient anxiety.

Rate of insulin administration will be the main driver for shifts in electrolytes

alongside initiation of the enteral feed. Frequency of monitoring of electrolytes

should be based on clinical judgement and reflect levels that would be

https://www.legislation.gov.uk/ukpga/1983/20/contents




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provided to those without type 1 diabetes as a minimum. Protocols for the

provision of refeeding vitamins should also be mirrored.

Nasogastric tube feeding Most settings will have had little experience of managing patients in this particular

scenario and a multidisciplinary approach is recommended in the management of

this complex situation.

The guidance around the use of nasogastric tube feeding in anorexia is already

discussed elsewhere but considerations specific to this particular patient group are

considered here.

Principles and competences

It is recommended that this is managed only where a highly skilled

multidisciplinary team approach can be implemented. The team should

include: a diabetes consultant supported by a specialist diabetes team, an

eating disorders consultant, a nursing team with knowledge and skills of

managing both enteral feeding and type 1 diabetes and specialist dietetics

with experience in both enteral feeding and type 1 diabetes.

Patients receiving enteral tube feeding in SEDUs need to be medically stable.

As well as demonstrating competency in the delivery of nasogastric tube

feeding, staff need to be proficient in the following key areas adapted from the

Diabetes UK position statement(14):

o A working knowledge of the correct administration of subcutaneous

insulin.

o A working knowledge of the monitoring of type 1 diabetes.

o A working knowledge of the action of different insulin products.

o Knowledge of the definition and clinical signs of hyperglycaemia and

hypoglycaemia.

o Awareness of unit protocols to manage hyperglycaemia and

hypoglycaemia.

o Knowledge of the circumstances in which the diabetes team should be

contacted.

o Understanding of how to supervise the self-administration of insulin (to

avoid manipulation of insulin doses).


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Insulin regime prescribed will be dependent on mode of delivery of the feed

and should be advised by a senior member of the diabetes team based on

published clinical guidance(14) and clinical expertise.

Due to the complexity of the clinical situation, it is recommended that staff

administer the insulin regime. Independence of the person with T1DE around

insulin administration is unlikely to be appropriate or safe at this point in

treatment.

Ready access to the diabetes team for clinical review is required. Pre-specify

the thresholds and pathways at which the medical team and or on-call or

diabetes team must be contacted out of hours, because not all ward staff may

know which blood glucose or ketone levels might be dangerous.

Clear guidance on blood glucose monitoring is required and must be dictated

by clinical need rather than ward routine(14).

Clear protocols for the management of hypoglycaemia need to be in place,

including if insulin has been administered and the feed is subsequently

stopped unexpectedly (e.g. due to nasogastric tube being pulled out or

removed) (see Biochemical risks in this annexe).

If post-bolus feed hypoglycaemia is a risk, the protocol may include giving

insulin in reduced doses after the feed to minimise the risk of hypoglycaemia.

Hypoglycaemia is also a risk if the patient self-induces vomiting after a

nasogastric bolus (or vomits after an adjunct meal or snack).

Treatment of hypoglycaemia may need to include feeding under restraint to

treat the hypoglycaemia if insulin has already been given.

Clear protocols for the management of hyperglycaemia and ketosis need to be

in place (see Biochemical risks in this annexe).

Clear guidance on when to escalate to the medical team is required in relation

to hypoglycaemia, hyperglycaemia and ketosis.

Consideration needs to be given to the potential for both feed and insulin to

be delivered under restraint (see Use of the Mental Health Act in this annexe)

and clear protocols developed should this be required.

Consider the training requirements of medical ward staff on use of the Mental

Capacity Act and Mental Health Act for these purposes and provide clear

guidelines in the context of T1DE.


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Consider the training requirements of staff on diabetes management,

including the administration of insulin, recognising and treating

hypoglycaemia, capillary blood glucose checks and ketone checks. Staff

training would include an understanding of risks associated with patients

potentially tampering with either/both nasogastric feeds and insulin infusions,

particularly if these are administered continuously rather than as bolus.

Medical management while nasogastric tube feeding

Evidence to support specific glucose levels during nasogastric tube feeding is

weak(15) and does not exist for this patient cohort. A blood glucose level of 6–

12 mmol/L has been proposed as an appropriate target for the management of

diabetes during enteral feeding(14) but in this cohort we propose an initial level of

insulin infusion sufficient to switch off ketones is the immediate priority with an

ongoing gradual increase in insulin to achieve a level of 10–17 mmol/L initially (with

ketones less than 0.6 mmol/L). The recommended ongoing rate of reduction in blood

glucose levels is unknown but should be slow enough to prevent complications

induced by rapid reductions in average glucose levels (see Biochemical risks in this

annexe) but sufficient to allow adequate nutritional supplementation and weight

gain (expert opinion).

There are two potential options for insulin administration:

1. Long-acting basal analogue insulin started immediately upon start of

nasogastric tube feed and continued once (or twice) daily plus an intravenous

variable rate insulin infusion (with hourly blood glucose checks and a sliding

scale) to maintain the insulin and ketone parameters above. Appropriate

doses need determination by the medical multidisciplinary team prior to

starting the nasogastric tube feed.

2. Insulins are administered subcutaneously to match the regime of the feed, i.e.

continuous, intermittent or bolus and should follow the principles set out in

the Diabetes UK position statement(14) but with reduced insulin

administration as described above. It is essential that these decisions are made

by collaboration between experienced diabetes teams and dietitians, with

regular review.

As in oral refeeding there is little guidance around the starting dose of insulin

alongside nasogastric tube refeeding. We have some experience of using insulin at a

total daily dose of 0.2–0.3 units/kg body weight as an initial oral refeeding/re-

insulinisation protocol without significant detrimental shifts in electrolytes,


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hypoglycaemia or development of ketosis. For T1DE patients being fed by nasogastric

tube, we recommend that the starting doses of insulin are decided under close

supervision of a senior member of the diabetes inpatient team with a dietitian and a

physician with clinical responsibility for the patient.

The ongoing insulin protocol will be dependent on the enteral feeding protocol;

continuous, intermittent or bolus and should follow the principles set out in the

Diabetes UK position statement(14). Any adjunct meals or snacks must also be

considered.

Frequency of blood glucose and ketone monitoring will be dependent on the enteral

feeding protocol; continuous, intermittent or bolus and should follow the principles

set out in the Diabetes UK position statement(14).

People with type 1 diabetes are at risk of hypoglycaemia following insulin

administration if the nasogastric tube feed is stopped for any reason (blockage or

removal of the tube) or if the feed (or any adjunct meal or snack) is purged. Under

these circumstances, regular monitoring of blood glucose in line with the principles

set out in the Diabetes UK position statement, with availability of intravenous 10%

glucose is essential(14). People with type 1 diabetes and low BMI/%mBMI are at

particularly high risk for severe hypoglycaemia (needing third-party assistance) due

to reduced glycogen storage in liver and skeletal muscle; the treatment

with intramuscular glucagon will not be very effective (although it remains part of

emergency treatment plan of severe hypoglycaemia) and must be followed up with

adequate carbohydrate replacement.

Use of diabetes technology

People on insulin infusion devices (insulin pumps) including those admitted for

nasogastric tube feeding should be switched to subcutaneous multi-dose insulin. In

exceptions, the insulin pump use can be continued on the ward, provided that ward

staff supervising the insulin replacement on the ward around the clock have been

adequately trained (completed competences on diabetes management e.g. TREND-

UK (Training, Research and Education for Nurses in Diabetes UK) framework(16), the

diabetes team has confirmed that the service user can use his device safely and the

diabetes team regularly reviews downloads and settings; to prevent ketoacidosis due

to cannula/infusion set problems, a low dose of long-acting basal insulin analogue

alongside the insulin pump therapy can be considered.

Consider fitting a flash continuous glucose monitoring system for closer and less-

invasive glucose monitoring (provided subcutaneous fat tissue allowing sensor


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insertion and not impacting on patient’s distress) with the option for remote

monitoring (which can be useful for liaising with the diabetes team for dose titration

advice)

Cardiovascular health/electrocardiogram

Given that eating disorders in children, young people and adults with type 1 diabetes

can be associated with blood glucose levels above recommended targets(17), adults

with T1DE can be predicted to be at increased risk of cardiovascular disease (CVD)

including heart disease, stroke and peripheral vascular disease. Risk factors for

cardiovascular health and assessment for cardiovascular and other macrovascular

complications should therefore form part of the medical assessment in T1DE.

Alongside working with a child, young person with their family or adult with T1DE to

optimise their blood glucose levels, other steps can be taken in adults to reduce the

risk of CVD including keeping blood pressure and cholesterol at recommended levels

and working with the person to manage other modifiable risk factors such as

smoking and physical activity, taking into consideration the risk that exercise may be

used as a compensatory behaviour in T1DE. Routinely these measures should be

started after the age of 40 for all patients with type 1 diabetes but should be initiated

earlier if other risk factors are present(17). However, a person with T1DE may find

additional medications stressful, while trying to cope with incrementing insulin

doses and careful prioritisation (and potentially deferring additional CVD prevention

medication to a later time in the therapy progress) with consensus of the patients’

needs to be undertaken here.

Hydration/oedema

Dehydration is more likely to be seen in those with raised blood glucose and ketone

levels and can rapidly lead to medical crisis through circulatory insufficiency and

acute kidney and hepatic injury. The risk of DKA is increased in those with type 1

diabetes with profound fluid loss. All patients should be fully assessed for

dehydration:

Take a corroborative history for fluid intake and signs of decompensation

(dizziness/fainting).

Undertake physical examination to include assessment of skin turgidity and

lying and standing blood pressure.


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Check electrolyte levels for high urea, creatinine, sodium and potassium.

In the absence of DKA oral replacement is preferable.

In those with eating disorders, excessive water ingestion may occur for several

reasons including a deliberate attempt to falsify weight, to mask hunger or because

of difficulty differentiating between thirst and hunger. In these instances, a dilutional

hyponatraemia is likely, although selective serotonin receptor inhibitors have been

described to cause Syndrome of Inappropriate ADH (SIADH) as a side effect. In those

with T1DE however increased thirst may be a sign of volume depletion and fluid loss

from hyperglycaemia due to insufficient insulin to meet requirements. A concern

about increased water ingestion should therefore be investigated carefully to

understand the underlying cause so that this can be appropriately addressed. A fluid

input/output chart should be kept, and daily electrolyte monitoring may be

necessary in the initial phase of early stabilisation to monitor fluid balance.

In the event that excessive water ingestion is thought to be behavioural and not due

to hyperglycaemia or an underlying medical condition such as diabetes insipidus

(lack of anti-diuretic hormone or renal resistance to anti-diuretic hormone), then

careful discussion with the individual should take place with goals to try and slowly

reduce their water ingestion to a more reasonable total daily volume (e.g. 2.5–3 litres

a day or using the Holliday-Segar equation in children and young people).

In the case of thirst as a response to hyperglycaemia, fluids should not be restricted

as this will increase the risk of DKA developing, particularly if ketones are present.

Instead, the priority should be on improving the hyperglycaemic picture.

In addition to other factors, in those with T1DE, consideration should be given to the

possibility that oedema can occur with the reintroduction of insulin. It is important to

physically examine the patient with oedema to rule out or treat other underlying

medical causes that may have been unmasked by the rehydration

(e.g. cardiomyopathy), including lung auscultation and echocardiography or chest x-

ray when clinically indicated. A careful documentation of the fluid input and output

balance is also helpful to monitor the oedema. While usually medically harmless, the

potential psychological impact on the person with T1DE that the increase in weight

and change in body shape from oedema can cause needs to be acknowledged and

support provided for the person to continue with their treatment goals.


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Biochemical

Insulin regulates how the body uses and stores glucose, protein and fat. In type 1

diabetes the absolute deficiency of insulin results in a switch to a catabolic

metabolism with increased breakdown of fat, protein and glycogen, which will also

result in weight loss. The resulting production of ketone bodies as alternative fuel

from fat breakdown causes increasing metabolic acidosis to the point of metabolic

decompensation (DKA), which constitutes a medical emergency, often needing

intensive care treatment.

Insulin regulates how the body uses and stores glucose and fat. In type 1 diabetes the

absence of endogenous insulin results in a switch from carbohydrate to fat

metabolism. The resulting production of ketones, if left unchecked, will result in,

among other things, rapid weight loss due to the breakdown of the body’s fat stores.

In T1DE a person with diabetes may deliberately and regularly reduce or miss their

exogenous insulin replacement with the specific aim of reducing weight or avoiding

weight gain. This puts both their short- and long-term health at significant risk due

to the consequences of the resulting hyperglycaemia and ketosis(2, 18, 19).

Management of hyperglycaemia in T1DE

Standard care of those with type 1 diabetes would aim to keep blood glucose

readings between 4–10 mmol/L both before and after meals with 70% of blood

glucose readings meeting this range (time in target)(20). For those with insulin

omission, giving physiologically appropriate amounts of insulin may cause

psychological distress as it is likely that giving insulin will be equated with putting on

weight. A stepped approach, gradually increasing the frequency and dose of insulin

administered is therefore recommended. This will allow time for psychological

adjustment and reduce the risk of treatment-related complications including

potential electrolyte shifts resulting from re-insulinisation (see BMI/starvation in this

annexe) and treatment induced deterioration of pre-existing retinopathy and

neuritis(12, 13) which can occur if blood glucose levels are reduced rapidly.

Treatment induced retinopathy diabetic retinopathy refers to damage of the blood vessels in the back of the eye

(retina). The most important factors linked with early worsening of retinopathy are

the severity of pre-existing diabetic retinopathy at baseline, and a large reduction in

HbA1c(21–23). Retinal screening and assessment should ideally have occurred prior to


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initiating treatment to achieve tighter glycaemic control with regular follow-up

screening visits planned(23).

Neuritis (treatment induced neuropathy of diabetes) Insulin neuritis is a form of acute neuropathy. It presents as neuropathic pain,

symptoms of autonomic dysfunction or a combination of both. Symptoms may

include burning or shooting pains in the extremities (but may be more generalised)

and orthostatic hypotension or syncope (fainting). As insulin neuritis can lead to

severe, disabling pain, there should be a focus on controlling symptoms while they

gradually improve over the subsequent weeks or months.

To reduce the risk of these complications occurring it is recommended that

glycosylated haemoglobin (HbA1c) is not reduced any faster than 20 mmol/mol (2%)

in 2 months(24, 25). The ‘normal’ blood glucose targets are therefore temporarily

relaxed. Initial insulin doses are not intended to return the blood glucose levels back

to ‘normal’ but it does serve to switch off the production of ketones reducing further

weight loss and reducing the risk of DKA. It is acknowledged that it may feel very

uncomfortable for health care professionals to accept these high glucose levels

however it is a temporary measure with the aim of progressively increasing insulin

doses to achieve recommended glucose targets. Screening for vitamin B12 and folate

deficiency and multivitamin replacement should be part of standard treatment

protocols in this group.

Management of raised ketones in T1DE Insulin deficiency is associated with the accumulation of ketoacids in the extra-

cellular fluid and a loss of bicarbonate anions in buffering to compensate the

metabolic acidosis. The resulting metabolic acidosis can result in DKA which is

associated with significant morbidity and mortality. Sick-day rules are commonly

used to curtail or avert DKA and national guidance for those with type 1 diabetes to

prevent DKA is available(16). In people with T1DE ketones also arise from prolonged

starvation, thus further increasing the risk of DKA. Measuring blood pH and

bicarbonate levels is essential to differentiate DKA from starvation ketones.

For those omitting insulin to manage their weight, following this guidance in full and

taking appropriate doses of insulin to correct ketones may be challenging, or refused,

even when they know it is for their own health and wellbeing. Some patients even

take inappropriately large doses of short acting insulin to avert having to go into

hospital for DKA treatment, which can result in severe hypoglycaemia. In many cases

DKA can be averted by preventing blood ketones rising above 1.5 mmol/L(13) and the


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health care professional may need to accept that giving smaller doses of insulin than

is usually recommended may be necessary with the revised aim being to reduce

ketone levels to a point that prevents DKA and keeps the person with diabetes safe

while accepting it does not eliminate ketones to a level usually recommended,

e.g. 2 units of rapid-acting insulin for ketone levels >1.5 mmol/L with repeat

monitoring of ketones and blood glucose levels at 1 hour. This is not recommended

best practice but the person with diabetes may feel able to accept this regime where

the full recommended insulin dose would be refused. In children and young people

this principle can also apply, but it may be necessary to be less compromising and

offer more medically appropriate adjustment doses (up to 0.1 x total daily dose).

Training for staff on the rationale for the gradual treatment approach described

above is required. Without this the levels of hyperglycaemia and ketones that are

likely to be present at the beginning of treatment can cause considerable anxiety for

staff caring for the person with diabetes and might also trigger routine pathways for

transfer into acute care, particularly in mental health settings. Clear treatment

protocols for the management of hyperglycaemia and ketones specifically designed

for this cohort of patients are therefore essential. An example inpatient management

plan for this purpose can be found in Appendix B.

Monitoring of blood glucose level and ketones Measurement of blood glucose and ketones using blood glucose and ketone meters

are recommended in preference to urine testing strips.

Use of flash glucose monitoring can be helpful in the treatment of T1DE. Results from

this method of monitoring correspond closely with capillary blood glucose readings

and is approved to dose insulin without the need for an accompanying finger prick

(except for flash glucose monitor readings below 4.0 mmol/l, readings that are

discrepant to clinical symptoms, or sensor malfunction). Data from the sensor can be

uploaded and shared with healthcare professionals and allows for remote specialist

advice, which is beneficial for multidisciplinary working, particularly in SEDUs.

Some glucose monitoring systems are also equipped with alarms which can identify

hypoglycaemia and offer reassurance to those with T1DE who are fearful of

hypoglycaemia. The reduced need for finger prick testing to ascertain blood glucose

readings can also reduce diabetes-related distress and be helpful for those with

needle phobia. The decision as to whether continuous glucose monitor systems are

supportive of recovery has to be taken on a case-to-case basis, as diabetes distress

can increase; e.g. some patients are alarmed by high blood glucose levels they see on


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their continuous glucose monitor system in the erroneous belief that high blood

glucose levels cause weight gain. (See Other mental health diagnoses in this annexe).

Management of diabetic ketoacidosis Guidance for treating DKA has been published by the Joint British Diabetes Societies

Inpatient Care Group(26). There is universal agreement that the most important

initial therapeutic intervention in DKA is appropriate fluid replacement along with

insulin administration. The highest mortality in DKA is related to potassium

abnormalities. Treatment with insulin promotes uptake of potassium intracellularly

which can lead to hypokalaemia which is a potentially life-threatening complication

during the management of DKA. Resolution of DKA is when blood ketones

<0.6 mmol/L and venous pH >7.3(26). Blood glucose levels will reduce as the ketones

reduce. Some local treatment protocols with fixed insulin rates are calibrated for

normal weight adults, resulting in fast drops of blood glucose in underweight people

with T1DE and will have to be modified on a case-to-case basis. It should be noted

that gradual reduction in blood glucose is essential as this is a critical window for

primary prevention of acute neuropathy. In children, standard guidelines are weight-

based and would therefore apply.

Hypoglycaemia and hypoglycaemia unawareness

Medical hypoglycaemia is defined as a blood glucose level of <4.0 mmol/L

(<3.5 mmol/L is now used in adults, but not in hospital). If left untreated it can

progress to loss of consciousness, collapse and death. Hypoglycaemia is more likely

to be seen in those with T1DE who administer insulin but use carbohydrate

restriction and/or excessive exercise as the primary mechanisms for controlling

weight.

Causes of hypoglycaemia in those with type 1 diabetes are described elsewhere. In

those with T1DE, additional causes may be implicated if insulin is being administered

including low glycogen stores as a result of carbohydrate restriction, low BMI/%mBMI

or excessive exercise, delayed gastric emptying as a result of diabetes-related

gastroparesis and/or starvation, purging, overcompensation with insulin following a

binge, increased sensitivity to insulin as a result of excessive exercise and low

carbohydrate diets.

Management of hypoglycaemia in T1DE

the factors outlined above that increase the risks of hypoglycaemia need to be

addressed within the management of T1DE. Standard treatment guidelines for

hypoglycaemia are described elsewhere. It is important to recognise that those with


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T1DE may refuse any or adequate oral treatment of hypoglycaemia due to fear of the

calories that will be consumed, putting them at risk of recurring episodes of

hypoglycaemia or the need for alternative methods of treating their hypoglycaemia

such as intravenous dextrose. People with type 1 diabetes have to have access their

hypoglycaemia treatment at all times, which can represent challenges around

managing binge eating and deliberately induced ketosis. It may be helpful to

prescribe medicalised hypoglycaemia treatment (glucose in liquid or gel form and

pre-portioned) to help avoid bingeing on hypoglycaemia treatment food items.

Clinicians should also be aware that a glucagon injection may not have the desired

effect of raising blood glucose levels and would not be a recommended treatment

under the following circumstances due to the potential for glycogen stores to be

reduced:

recurrent hypoglycaemia

periods of sickness involving vomiting, diarrhoea and loss of appetite

eating no or very little food

chronically low carbohydrate intake

excessive exercise

low BMI/%mBMI

repeated purging.

A person with T1DE may also request glucagon as a hypoglycaemia treatment, to

avoid ingesting the calories in oral hypoglycaemia treatments. This however is not

recommended if oral treatment is clinically indicated as it will leave glycogen stores

depleted.

An example plan for the management of hypoglycaemia, including pseudo

hypoglycaemia for use inpatient settings can be found in Appendix B. On SEDUs,

guidance should also be available clearly indicating when transfer to an acute

hospital setting for the treatment of hypoglycaemia is required.

Hypoglycaemia unawareness

Those who experience episodes of severe or recurrent hypoglycaemia can lose their

symptom awareness of hypoglycaemia, meaning they will no longer be able to

detect when their blood glucose levels drop below 4 mmol/L. This will put the person

at increased risk of requiring external assistance for recovery. Hypoglycaemia

awareness may be partially restored by avoiding further hypoglycaemia and for this


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reason people with diabetes are encouraged to aim for their blood glucose levels to

remain above 4 mmol/L, with the commonly used motto ‘make four the floor’(2, 3). To

achieve this, psychological work may be required, e.g. to address fear of

complications or challenge the perfectionism trait often seen in eating disorders with

an alternative ‘good enough’ approach(5).

Pseudo (or false) hypoglycaemia

If a person with T1DE has been running high blood glucose levels for a prolonged

period, they may experience symptoms related to hypoglycaemia at normal or high

blood glucose levels, particularly when insulin is re-introduced and blood glucose

levels begin to decrease. Blood glucose monitoring is essential to be able to

distinguish a pseudo hypoglycaemic episode from medical hypoglycaemia where

the blood glucose is <4 mmol/L. Treatment for pseudo hypoglycaemia should be

conservative, i.e. encouraging rest, offering reassurance and re-checking blood

glucose levels 10 minutes later. However, for symptomatic relief or to manage

associated anxiety, if blood glucose levels are between 4–12 mmol/L, a small dose

(e.g. 5 g) of rapid release carbohydrate can be offered. It is important not to over-treat

pseudo hypoglycaemia because repeated treatments will result in maintaining the

status quo rather than enabling adjustment to the reduction in blood glucose levels.

Over treatment of pseudo hypoglycaemia may also be used in a deliberate attempt

to maintain high blood glucose levels and ketones to achieve an ongoing weight-

losing state. It is important to note that experiencing pseudo hypoglycaemia can

produce the same psychological responses as typical hypoglycaemia, such as fear

and anxiety.

Acid-base changes

Changes in acid-base balance observed with misuse of laxatives (typically a

metabolic acidosis) or with vomiting and diuretic use (typically metabolic alkalosis)

can be further complicated by the acidosis resulting from the accumulation of

ketoacids that occurs with insulin omission. In T1DE a range of different acid-base

balances can therefore be seen and in some instances a mixed picture may be

present.

Electrolyte imbalance

Important clinical factors that contribute to electrolyte imbalance in T1DE include:

the use of laxatives

purging


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increased fluid intake

hyperglycaemia causing pseudo-hyponatraemia

the use of SSRI

malnutrition/malabsorption

vomiting due to gastroparesis.

The potential for renal impairment, as a complication of type 1 diabetes to impact on

the biochemical picture should be considered and assessment of renal function

should form part of the medical assessment in T1DE. The first sign of nephropathy

may be microalbuminuria. Screening and calculation of albumin: creatinine ratio in

type 1 diabetes is recommended(8). Early nephropathy is usually treated with an

angiotensin-converting enzyme inhibitor and by improved blood glucose and blood

pressure management. Management of chronic kidney disease is described

elsewhere(8). In the acute crisis presentation of T1DE, acute kidney failure due to

severe dehydration following hyperglycaemia induced glucosuria is often the

dominant picture. Malnutrition can also influence renal markers (e.g. low creatinine).

Medication

Because of the associated weight loss, gastrointestinal symptoms and risks of

hypoglycaemia and DKA we recommend that these adjunct therapies should be

used with caution in those with T1DE.

Glucagon-like peptide 1 (GLP-1) agonists and sodium-glucose cotransporter-2 (SGLT-

2) inhibitors have, in some studies, been demonstrated to reduce HbA1c, body weight

and total daily doses of insulin when used by people with type 1 diabetes alongside

insulin(27).

GLP-1 agonists have however been associated with gastrointestinal side effects(28),

which may be counterproductive for the recovery of a person with T1DE who tries to

avoid purging by vomiting or has got gastroparesis.

SGLT-2 were associated with a greater risk for DKA and volume depletion, particularly

euglycaemic DKA where ketones and acidosis are present but at a much lower

glucose level which can make identification and treatment difficult(27). SGLT-2

inhibitors are contraindicated in people with T1DE due to the increased risk for DKA

in this group.


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Where those with T1DE are already prescribed these medications the physiological

and psychological risks of continuing or discontinuing them needs to be carefully

considered in conjunction with the person with T1DE.

Metformin also has gastrointestinal side effects and can be used to promote weight

loss. It should be used with caution.

Other medicines

Olanzapine is commonly used at low doses in the management of eating disorders. It

can be associated with insulin resistance, but the effect is rarely clinically significant.

There should be no diabetes contra-indications for the use of other psychotropic

medicines.

Disordered eating behaviours

Food restriction

In presence of appropriate insulin administration food/carbohydrate restriction will

result in the same risks as for those with restrictive anorexia nervosa. There is the

potential for an increased risk of hypoglycaemia if insulin is not appropriately

adjusted (see Hypoglycaemia in this annexe). Food restriction also results in

starvation ketones, further increasing the risk of DKA.

Food restriction alongside omission or restriction of insulin will result in risks

increased beyond those of restrictive anorexia nervosa as the availability of calories to

the body will be further reduced.

Excessive carbohydrate consumption

Excessive carbohydrates may be consumed to keep blood glucose levels and ketones

high, to promote weight loss, and is described in more detail below (see

Compensatory behaviours in this annexe).

Bingeing

For those with T1DE bingeing will have risks beyond those without T1DE. Without

additional insulin being administered blood glucose levels will rise and ketones may

ensue. Conversely guilt, shame or fear of complications after an episode of bingeing

and may result in overcompensation with a large dose of insulin, potentially causing

hypoglycaemia(29). Where the person is driven to engage in compensatory


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behaviours after a binge as such as restriction, purging and excessive exercise the

challenge of stabilising blood glucose levels is further complicated.

In the context of pre-existing gastroparesis there is a small but real possibility that

bingeing may lead to may lead to gastric dilatation, ischaemia and.

Diabetic gastroparesis

Where it is present diabetic gastroparesis can result in food patterns, behaviours and

symptoms that may mirror or maintain eating disorder pathology including early

satiety and bloating, loss of bowel motility and poor dietary intake with associated

weight loss. It should be included in the medical assessment of those with T1DE and

its management is summarised elsewhere. Gastroparesis can also be transient in the

context of sustained hyperglycaemia, therefore assessments for gastroparesis

diagnosis should be conducted once blood glucose levels are normalised. In a person

with a binge-purge pattern eating disorder it can be difficult to differentiate to what

extent vomiting is due to gastroparesis and to what extent it is self-induced. Adjunct

treatment with antiemetics may be considered.

Activity and exercise

The impact of exercise on risk of hypoglycaemia and ketosis are described elsewhere

(see Biochemical risks and Compensatory behaviours in this annexe). Physical activity

in the presence of incipient DKA can accelerate metabolic deterioration. Over-

exercising can also contribute to hypoglycaemia risk and to weight loss.

Exercise can result in friction burns, bruising and blisters, cracked or dry skin and

increased callous formation on the feet. In those with T1DE the risk to foot health is of

particular concern due to the circulatory and neurological complications potentially

associated with both type 1 diabetes and starvation if it is present. Fracture risk will

also be increased in patients with reduced bone density. Foot assessment should

form part of the medical assessment in those with T1DE including checks for signs of

circulatory and neurological deficit. More information on diabetic foot care can be

found elsewhere(9, 30).

Compensatory behaviours

The risks associated with compensatory behaviours will mirror those of other eating

disorder presentations. Additional considerations relating to T1DE follow.


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Insulin omission or reduction

When challenged to address the omission or reduction of insulin those with T1DE

may engage in a range of strategies to disguise this behaviour (see Table 2). This list is

not exhaustive. Over checking of blood glucose and ketone levels to gain

inappropriate reassurance that a weight-losing state is maintained may also occur.

Consideration needs to be given as to how best the person with diabetes can be

supported to address these behaviours:

Staff should have a good working knowledge of insulin administration.

Staff should be aware of the potential ways in which insulin omission can be

disguised.

Insulin should be stored safely at an appropriate temperature to prevent

deliberate deterioration.

In the initial stages of treatment, it is suggested that equipment, including

pens, needles and meters should be stored in a clinical area to minimise the

risk of deliberate damage, tampering or misuse and spare equipment should

be readily available in the event of damage or loss.

Staff should closely supervise insulin administration at least in the initial stages

of treatment. It is our experience that close supervision is preferable to staff

administration of the insulin however be guided by the individual situation.

As a general principle we would advocate pens rather than pump for insulin

administration. This facilitates staff confidence in settings where the

complexities of managing a pump may be challenging for non-diabetes

specialist staff. Attempts to avoid insulin administration by the person with

diabetes are also more easily identified and therefore the person can be better

supported to give the advised dose.

Staff should be aware that the anxiety of insulin administration will be akin to

that of eating food in those with other eating disorder presentations. Anxiety

will therefore be high at the times when insulin is administered. Allowing time,

taking an empathic approach and reassurance are key.


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Table 2: Strategies for insulin omission/reduction (not exhaustive)

Strategy

Secrecy Injecting insulin in private/away from others.

Insulin Leaving insulin in a warm environment to deteriorate, thereby reducing its

effectiveness.

Pens Leaving diabetes equipment elsewhere.

Dialling up a smaller dose of insulin or dialling down dose just before injection.

Omitting to ‘prime’ the insulin pen resulting in the delivery of a reduced dose of

insulin.

‘Squirting’ the insulin prior to placing the needle into the injection site.

Injecting insulin into sites where lipoatrophy is present to reduce the absorption

of insulin into the body.

Not fully depressing the insulin pen plunger.

Releasing the plunger or pulling out the needle from the injection site before the

end of the full 10 seconds required to deliver the full dose of insulin.

Continuing to pinch up the skin after injection to squeeze insulin out.

Injecting the insulin into clothes.

Bending needle just before injection or not attaching needle properly.

Leaving insulin on the radiator/in the sun to denature.

Pumps Taking the pump off and not reconnecting it.

Turning the pump off – disabling the alarm.

Incorrect siting of the cannula resulting in a reduced or no delivery of insulin to

the infusion site.

Making a hole in the tubing from which the insulin can drip out.

Altering the ratio doses programmed into the pump.

Falsifying blood sugar readings in order that the pump does not advise a

correction dose.

Reducing the amount of carbohydrate entered to avoid the pump advising as

much/any insulin.

Changing the pump settings to facilitate under dosing of insulin, e.g. falsifying

the time of insulin doses given so it appears that insulin remains on board.

Meters Making up solutions using sugary substances and using this to falsify blood

glucose readings to be lower, to avoid a correction dose.


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Frequent checking that ketones are present and if not taking steps to increase

carbohydrate/decrease insulin.

Using control solution, adding alcohol to test strips to obtain false low readings.

Example flow charts for the management of both long and short acting insulin

refusal can be found in Appendix C. An example protocol for returning autonomy of

insulin administration to the person with diabetes is also available in Appendix D.

As well as omitting insulin, other strategies may be employed to increase blood

glucose levels and/or achieve a ketotic state with the purpose of achieving loss of

body fat and weight. This puts at high risk for DKA, though many are able to

maintain a subclinical state of ketoacidosis to avoid admission. These strategies

include:

Overconsumption of high carbohydrate foods and drinks alongside insulin

omission may be present at diagnosis or may emerge as insulin is restarted to

try to maintain the presence of raised blood glucose and ketone levels.

Support should be provided to challenge this pattern of carbohydrate

consumption and consideration given to access to high carbohydrate foods

including sugar and high sugar drinks which are often readily accessible in

inpatient environments. Overconsumption of hypoglycaemia treatments may

also be used for this purpose. Overconsumption of high carbohydrate foods

and drinks can also be triggered by pseudo or real hypoglycaemia that induce

hunger and adrenergic symptoms as part of the counterregulatory response.

In a person without enough circulating insulin, exercise will raise blood

glucose levels and increase ketone production(29) therefore exercise may be

used in T1DE as a method of maintaining raised blood glucose and ketone

levels. Fluid losses resulting from exercise will further progress the

ketonaemia, increasing the risk of DKA. Support to challenge this potentially

dangerous pattern of behaviour may therefore be needed, and consideration

given to raised ketones as a potential consequence of covert exercise,

particularly in the early stages of treatment when for the reasons described

above insulin doses will be small (see Biochemical risks in this annexe).

Emergence of other eating disorder behaviours

Those with T1DE who are omitting or restricting insulin may present atypically,

appearing relaxed around food choices and not engaging in other compensatory

behaviours. Insulin reintroduction may result in the emergence of compensatory

behaviours not previously observed, as the person’s focus on how they can control


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weight and shape shifts elsewhere. Clinicians, particularly in inpatient settings where

insulin administration is closely supervised should be alert to the emergence of

behaviours more typical of other eating disorder presentations such as restriction,

covert exercise and purging. Clinicians should also be aware of the potential for

alternative self-harm behaviours to emerge and for deterioration in mood and

increased anxiety symptoms (see Other mental health diagnoses in this annexe).

Vomiting

Can lead to unpredictable blood glucose levels, including the risk of hyperglycaemia

and hypoglycaemia and their associated complications (see Biochemical risks in this

annexe). This may be further complicated by insulin omission or restriction in those

with T1DE and in those who have gastroparesis. Clinical management of bolus insulin

around this may be giving split insulin boluses (lower insulin bolus before the meal

with a post-meal correction if the meal has been kept down) or low dose post-meal

injections.

Sham feeding

Other behaviours include sham feeding (chewing and spitting). Patients may over- or

under-estimate the amount of energy absorbed and thus be at risk of hypo or

hyperglycaemia. This behaviour is often experienced as deeply shameful and rarely

spoken about.

Engagement with the management plan

In those with T1DE barriers to engagement with the management plan will mirror

those of other eating disorder presentations. Additional considerations for T1DE

follow:

Previous experiences with health services

Negative past experiences with healthcare teams can present a significant barrier to

the engagement of this cohort. Contact and communication that reflects a

supportive, non-judgemental, encouraging and empathic approach, which

continues if avoidance of contact persists, is essential(6).

Language matters

Careful consideration and adjustment of the language used is key(31).


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Cognitive function

It is known that starvation has a significant impact on cognitive function(32) and that

refeeding is required for successful engagement in treatment plans and

psychological therapy. Similarly, both the presence of hyperglycaemia and

ketones(33) and severe or recurrent hypoglycaemia(34) have been demonstrated to

impact on cognitive function and therefore have the potential to interfere with

progression of treatment. Improvement in these aspects of diabetes management

are, therefore, important for engagement with the treatment plan.

Diabetes-related psychological concerns

Diabetes-related distress and other diabetes-related psychological concerns can

impact on progression of treatment (see Other mental health diagnoses in this

annexe).

Lack of insight Lack of insight has been described and reviewed for people with anorexia

nervosa(34–36). Research is lacking in relation to T1DE, but anecdotally it has been

observed and may contribute to a lack of engagement in treatment. The degree of

presenting risk must be assessed, and where medical or psychiatric risks are high

consideration given to capacity to consent to treatment (see Use of Mental Health

Act in this annexe). Lack of insight may also need to be considered in relation to

safeguarding of self and others, fitness to work and driving. The impact on carers can

also be considerable.

Family and carers

The ethos of diabetes care is often to encourage autonomy. In contrast, the ethos

within eating disorder services would be to encourage family and carers to offer

support to those with T1DE to address the challenges they face. Living with a person

with T1DE can cause anxiety; being faced with someone who is clearly unwell, who

may lack insight and shows little inclination to implement the obvious solution (to

eat and/or take their insulin) can drive strong emotional reactions which, in turn, can

play a part in the maintenance of the eating disorder. Consideration should therefore

be given to how families and carers can best be supported.


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Other mental health diagnoses

As well as being common comorbidities in eating disorders, depression and anxiety

also commonly occur in those with type 1 diabetes(37). Depression in those with

type 1 diabetes is associated with suboptimal diabetes self-management, raised

HbA1c levels and increased diabetes distress(38). The deterioration in metabolic

control that occurs in those with those with T1DE who restrict or omit insulin can

worsen depression(39). Anxiety may be overlooked in those with type 1 diabetes as

severe anxiety and panic attacks share some similar physical symptoms to

hypoglycaemia (e.g. sweating, increased heart rate, shaking and nausea).

Consequently, elevated anxiety symptoms may be misinterpreted by both people

with diabetes and health care professionals, resulting in anxiety disorders remaining

undiagnosed. From clinical observation, mental health co-morbidity and

hyperglycaemia can be intertwined: in some patients persistent and chronic

hyperglycaemia masks symptoms of their underlying depression or anxiety disorders

and symptoms seem to re-emerge when glycaemic management improves. This

makes frequent monitoring and re-assessment of the mental health status during

therapy mandatory.

Diabetes distress is the emotional distress resulting from living with diabetes and the

burden of the relentless tasks of daily self-management(40) as well as the social

impact of diabetes(41). It is observed to commonly coexist in those with T1DE.

Diabetes distress can present a significant barrier to recovery as it requires the

person to re-engage with all of the practical tasks and cognitive processing that is

required of living with type 1 diabetes on a daily and ongoing basis. Its psychological

treatment cannot be separated out from treatment of the eating disorder as the

benefits of not having to engage in these tasks serves as a powerful maintaining

factor in those who restrict or omit insulin to control their weight and shape.

Fear of medical hypoglycaemia (blood glucose level <4 mmol/L) is a specific and

extreme fear evoked by the risk and/or the occurrence of low blood glucose

levels(42). Being concerned about hypoglycaemia is rational and adaptive, but if this

develops into excessive fear it can result in the omission or reduction of insulin doses,

or in the overconsumption of carbohydrates to maintain blood glucose at a raised

level(5). It may therefore emerge as a barrier to the treatment of T1DE as blood

glucose levels normalise. Similarly, a fear of needles (or, in its extreme form, a needle

phobia) can pose an obstacle to improved diabetes management in people with


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T1DE. Conversely, a fear of complications can result in overly tight management of

blood glucose levels with its associated risk of severe or recurrent hypoglycaemia.

An overview of the identification, and treatment options to address the psychological

issues described above, can be found elsewhere.

Self-harm and suicide

There is limited literature on the risk of self-harm in T1DE, but it is reasonable to

assume that the potential for self-harm behaviours will mirror those of other eating

disorder presentations and their presence and management should be considered in

this patient cohort. If not present at diagnosis clinicians should be aware, as with

other eating disorder presentations, that they may emerge as weight and shape

concerns are challenged by treatment. The act of ongoing insulin omission and the

damage caused can also in itself be viewed as a form of self-harm(43). There is also a

clinical subgroup with comorbid emotional instability, self-harm or history of trauma

for whom insulin omission is a coping strategy

Suicide occurs more frequently with the coexistence of psychiatric and physical

illness(44). The increased risk of suicide in eating disorders is well-documented and a

systematic review on suicide risk and type 1 diabetes indicated that, in general, adult

patients with type 1 diabetes have a higher risk for suicide than the general

population(45). In addition, it has been found that young adults admitted to hospital

for DKA have an increased risk of being admitted to hospital for a subsequent suicide

attempt. The risk of a suicide attempt was highest in the 12 months following the

ketoacidosis episode(46).

It is vital to consider the risk of suicide in those with T1DE. Importantly those with

T1DE have access to insulin which can cause hypoglycaemia and subsequently death

if it is severe and lasts for a prolonged period of time. Health care professionals

working with those with T1DE must therefore be mindful of the potential for this

lifesaving drug to be used in a deliberate attempt to end life. A four-point plan for the

safe management of depressed adult patients prescribed insulin has been

proposed(47):

Regularly assess for symptoms of depression.

Refer to a mental health provider (sooner rather than later).

Work closely with the mental health provider.

Monitor thoughts of suicide when working with a patient with depression.


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If there are red-flag warning signs/immediate risk of suicidal behaviour, the

patient will require:

o immediate discussion with or referral to mental health services

o a robust safety plan

o adequate support

o removal of access to means.

The safety plan should be co-produced with the patient and should have explicit

reference to removal and/or mitigation of means to harm themselves. Mental health

providers will need to liaise with diabetes services to consider what realistic plans can

be put in place surrounding availability of insulin as a means of harm, e.g. insulin

injections under supervision only. The safety plan should list activities and coping

strategies and contain information on how to access social, psychological and

emergency support(44).

For children and young people, the ingredients will be the same, but early

involvement of local child and adolescent mental health services is recommended

for them to lead the care, supported by the children’s diabetes team who know the

young person and their family.

Use of the Mental Health Act

Because eating disorders can be accompanied by significant morbidity, especially if

insulin restriction is used as a compensatory behaviour, there may be occasions

when clinicians may consider using the Mental Health Act(48) in the context of T1DE

(e.g. when a patient's physical health or survival is seriously threatened as a result of

their mental illness).

The Mental Health Act section 63 (‘medical treatment’ in relation to a mental

disorder) refers to medical treatment the purpose of which is to alleviate, or prevent a

worsening of, the mental disorder or one or more of its symptoms or manifestations.

It applies only to medical treatment for the mental disorder and treatment for a

physical condition may only be given without the patient’s consent therefore, if it is

sufficiently connected to the treatment of the patient’s mental disorder.

Considering the above in relation to T1DE, it would seem permissible to compel a

person to receive treatment specifically for the management of their diabetes if it

would prevent a serious deterioration in their health. Prolonged hyperglycaemia and

https://www.legislation.gov.uk/ukpga/1983/20/section/63


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ketosis per will need to be taken into account during assessment as factors that

impact on cognitive functioning and therefore potentially also mental capacity.

In patients over the age of 16 it may also be possible to justify under the Mental

Capacity Act(49) action that is taken in an emergency as the minimum necessary to

prevent serious injury or loss of life. For those under 16 years, the Mental Health Act

applies.

Common law can be used to treat patients in emergencies if it is not possible to

perform a capacity assessment, e.g. if the patient is unconscious due to diabetes(50).


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Appendices

Appendix A: Example re-insulinisation and refeeding

protocol for people with type 1 diabetes and disordered

eatinga

All patients requiring support with re-insulinisation/refeeding should be considered

at risk of shifts in electrolytes with the reintroduction of insulin and/or carbohydrate.

Food

In the first instance the proposed fixed insulin doses will not match

carbohydrate intake therefore strict carbohydrate counting is not required(2).

An awareness of carbohydrate content at different meals is however

important to ensure the meal plan is safe and avoids unnecessary hypo/hyper

glycaemic states. Carbohydrate estimates are provided with the example

refeeding starter plan.

Those with T1DE may have selective concerns regarding the carbohydrate

content of their plan and may require reassurance to normalise the balance of

their intake. A daily carbohydrate intake of around 150 g is deemed

appropriate within the context of a starter refeeding plan.

Patients should have access to both quick and long-acting carbohydrate as

pre-defined treatment portions. Their consumption needs to be clearly

documented.

If eating more than the ½ portion plan do not reduce food intake, instead

continue with the person’s current dietary intake and follow the same insulin

protocol below. This is agreed as safe as the refeeding risk is mediated by the

amount of insulin provided, not by the amount of food.

Refeeding vitamins are recommended as outlined below and should be

started alongside the re-insulinisation/refeeding plan.

a The protocol outlined below has been developed by the ComPASSION TEAM. Dorset Health Care

University NHS Foundation Trust/University Hospitals Dorset NHS Foundation Trust.


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Multivitamin

Adults (18+ years): Multivitamin and mineral supplement, e.g. Forceval

capsule or Forceval soluble tablet: one a day

12–17 years: Forceval one tablet daily

1–12 years: Abidec 0.6 mL daily

Vitamin B

Vitamin B complex strong (one tablet contains 5 mg B1 [thiamine], 2 mg B2

[riboflavin], 20 mg nicotinamide and 2 mg B6 [pyridoxine])

Adults (18+years): two tablets three times daily (TDS)

12–18 years: three tablets TDS

1–12 years: two tablets TDS

Thiamine 100 mg BD

Adults (18+ years): 100 mg BD(51)

Under 18 years of age: (52) Evidence is lacking in the under 18s. Adult doses

can be used for older adolescents.

Note: If strong suspicion of thiamine deficiency: Pabrinex

Vial 1 (5 mLs contains B1 [thiamine] 250 mg and B2 [riboflavin] 4 mg, B6

[pyridoxine) 50 mg])

Vial 2 (5 mLs contains C [ascorbic acid] 500 mg, nicotinamide 160 mg, glucose

1000 mg)

Adult dose: 10 mL of each ampoule diluted with 50–100 ml of (0.9% saline or

5% dextrose) given over 30 minutes

Child dose:

6–10 years Third of the adult dose

10–14 years Half to two thirds of the adult dose

14 years and

over

Adult dose


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Once the ½ portion meal plan is established, aim to increase one meal to full

portion every 2–3 days to establish full portion breakfast, lunch and evening

meal. It should be acknowledged that some people will potentially

psychologically be unable to tolerate this speed of increase in food and the

plan adjusted accordingly.

For those not completing meals and snacks, nutritionally complete

supplements should be offered as an alternative, to manage the risk of

underfeeding and minimise the risk of hypoglycaemia and pseudo

hypoglycaemia. Amounts should be calculated based on approximations to

the meal or snack equivalent carbohydrate content. Note that some

nutritional supplements do not contain carbohydrate, e.g. Calogen (Nutricia)

and Fresubin 5 kcal Shot (Fresenius Kabi).

In the first instance the proposed fixed insulin doses will not match

carbohydrate intake therefore strict carbohydrate counting is not requiredb.

An awareness of carbohydrate content at different meals is however

important to ensure the meal plan is safe and avoids unnecessary hypo/hyper

glycaemic states. Carbohydrate estimates are provided with the example

refeeding starter plan.

Those with T1DE may have selective concerns regarding the carbohydrate

content of their plan and may require reassurance to normalise the balance of

their intake. A daily carbohydrate intake of around 150 g is deemed

appropriate within the context of a starter refeeding plan.

Patients should have access to both quick and long-acting carbohydrate as

pre-defined treatment portions. Their consumption needs to be clearly

documented.

Insulin

If omitting or taking only sporadic or minimal amounts of insulin, commence

initially on 10 units of long-acting insulin. Some negotiation may be required

around this initial dose, which can be calculated as approximately 0.2 units/kg

of body weight with planned incremental increases to meet the individual’s

requirements (expert opinion). This is alongside fixed doses of two units of

rapid-acting insulin for meals (initially no insulin with snacks).

b An alternative approach is to use carbohydrate to insulin ratios with, e.g., a starting insulin-to-

carbohydrate ratio of 1 unit of rapid-acting insulin to 20 g of carbohydrate.


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Ketones should be tested pre-meal if blood glucose is elevated (centres may

vary on the level at which they intervene) and if ketones are present follow the

hyperglycaemia/ketone management plan in Appendix B.

With each meal increase, aim for a doubling of initial insulin dose. It should be

acknowledged that some people will potentially psychologically be unable to

tolerate this speed of increase in insulin and the insulin plan adjusted

accordingly. Alternatively, the insulin-to-carbohydrate ratio can be adjusted in

a stepwise plan.

It is acknowledged that blood glucose will remain elevated in the first

instance, and this can be addressed after the refeeding period is completed,

with insulin increases being made at meals and introduced at snacks to

continue the process of reducing blood glucose levels gradually. See the

Insulin management plan in Appendix D.

Beyond the initial reintroduction of insulin and food, as blood glucose levels

normalise options include a fixed carbohydrate meal plan alongside fixed

doses of insulin OR the reintroduction of carbohydrate counting alongside

variable doses of insulin.

Monitoring

Flash monitoring is advised and will enable clinicians to monitor the change in blood

glucose and make gradual appropriate adjustments to insulin accordingly.

Although there can be a risk of electrolyte shifts up to a fortnight later in the

refeeding process, the risk is highest within the first 72 hours of initiating

refeeding(53). As a minimum, check refeeding bloods at baseline, day 2 and day 5,

then as clinically indicated.

In the absence of robust evidence, where re-insulinisation/refeeding is progressed

more rapidly or if other risk factors for the development of refeeding syndrome are

present such as infection or abnormal baseline electrolytes, increased frequency of

monitoring of electrolytes is advised based on clinical judgement and reflecting

levels that would be provided to those without type 1 diabetes as a minimum.

Local guidance for correcting blood levels if abnormal electrolytes are identified is

outlined in Table 3 below. Always seek consultant physician/paediatric, or

diabetologist or psychiatrist guidance on management if abnormal electrolytes are

identified.


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Weight should be monitored weekly. Significant upward shifts in weight during the

refeeding phase will reflect changes in fluid balance rather than a significant

increase in lean tissue and body fat. While this shift in fluid is usually medically

harmless the potential for psychological impact needs to be acknowledged and

support provided for the person to continue with the refeeding plan despite the

change in weight. Beyond the refeeding period more predictable weight change can

be anticipated as physiology normalises. Ongoing support with weight and shape

concern will be required.


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Table 3: Guidance for the correction of electrolyte abnormalities

Potassium

3.5–5.0 Normal range

3.0–3.4 Replace orally with Sando K (12 mmol K+ per tablet), 2 tablets BD–

TDS or 2 mmol/kg/d in divided doses in children and young people

<2.5 Requires intravenous replacement

Sodium

Standard guidance from main Guidance document applies – note

pseudohyponatraemia can occur in the context of hypoglycaemia

Phosphate


0.5–0.79 Replace orally with Phosphate Sandoz (16.1 mmol PO4 per tablet),

1–2 tablets BD

<0.5 Requires intravenous replacement – refer patient to acute care

Magnesium


0.5–0.69 Replace orally with magnesium citrate 150 mg (6.2 mmol/tablet).

Two tablets BD

<0.5 Requires intravenous replacement – refer patient to acute care

Support

Undertaking the proposed protocol can be challenging for those with T1DE. Barriers

to change include fear of weight gain and diabetes distress. Consideration therefore

needs to be given to how the person with diabetes can be supported.

Staff should be aware that the anxiety of insulin administration will be akin to that of

eating food in those with other eating disorder presentations. Anxiety will therefore

be high at the times when insulin is administered. Allowing time, taking an empathic

approach and reassurance are key.

It can be helpful to consider a staged approach, to support the person to move

forward with re-engaging with taking their insulin. A staged guide to achieving this

has been developed. See Appendix D.


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Refeeding starter planc

BREAKFAST Carbohydrate: 1 cup* Rice Krispies/Cornflakes, ¾

cup other cereal, or 2 Weetabix or Shredded

Wheat

26–34 g

(carbo-

hydrates)

Add some protein: ¾ cup semi-skimmed milk 8 g

MORNING SNACK: 1 cup semi-skimmed milk 11 g

LUNCH

Carbohydrate: 1 medium slice of bread or ½

bagel or 1 standard pita bread or 1 small jacket

potato (to fit in ½ the palm of your hand)

16.5–24 g

Add some protein: 1 ½ slices cooked

meat/chicken or ½ small can tuna/ baked beans

or 1 cheese circle or equivalent cheese portion, 1

egg or 1 individual pot of hummus.

Add some vegetables: small bowl salad

Add a fat source: 1 level tsp

butter/margarine/mayonnaise or salad cream

Include a second course, e.g.:

Dairy option: ½ standard pot of whole milk

yogurt (e.g. Müller Fruit Corner, Activia or Greek-

style) or ½ rice pudding/custard pot or 1 scoop of

ice cream.

6.5–11 g

Add some fruit: ½ a portion of fruit 3–10 g

AFTERNOON

SNACK: 1 cup semi-skimmed milk 11 g

MAIN MEAL:

Carbohydrate: ½ cup cooked rice, pasta,

spaghetti or couscous, 1 jacket potato (to fit

½ the palm of your hand) or 2 egg-sized

potatoes, 6 chips/wedges.

15–23 g

c Developed by the Wessex ComPASSION Team.


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Add some protein: ½ chicken breast or

equivalent meat portion, 1 rounded serving

spoon of Mince (1 ½ if a high vegetable

content), ½ baked fish fillet, 2 chipolata

sausages or fish fingers, 1 egg, 1 rounded

serving spoon Quorn pieces/kidney

beans/chickpeas/cooked lentils (1 ½ if a high

vegetable content).

Add some vegetables: ½ serving spoon of

vegetables, small bowl salad

Add a fat source: 1 tsp oil/1 level tsp butter or

margarine

Add a flavour source: e.g. a sauce, herbs,

spices, etc.

OR: ½ portion of a homemade mixed meal: 1 ½–

2 rounded serving spoons lasagne, shepherd’s

pie, pasta bake (includes the vegetable

portion).

18.5–

25.5 g

¼ of a whole regular size thin crust pizza, plus

a vegetable/salad portion.

Include a second

course, e.g.: 6.5

Dairy option: ½ standard pot of whole milk

yogurt (e.g. Müller Fruit Corner, Activia or

Greek-style), or ½ rice pudding/custard pot,

or 1 scoop of ice cream.

6.5–11 g

Add some fruit: ½ a portion of fruit 3–10 g

SUPPER SNACK: 1 cup semi-skimmed milk + 1 digestive biscuit 20 g

* Cup measures refer to UK measuring cups.

FLUIDS Aim for 6–8 mugs of fluid a day. Fluid requirements may be

higher in hyperglycaemia due to polyuria, patients may

need access to more water All fluid intake should be

recorded.


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Appendix B: Inpatient protocols for the management of

hyperglycaemia and ketones and the management of

hypoglycaemia in adultsd

d Developed by the Wessex ComPASSION Team.


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Appendix C: Inpatient protocols for the management of

refusal of short- and long-acting insulin in adultse

e Developed by and adapted from Wessex ComPASSION Project.


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Appendix D: Inpatient insulin management care plan for

adults with type 1 diabetes and eating disordersf

1. Stages of insulin management Select ()

2. Stages of insulin dosing Select ()

f Developed by and adapted by Wessex ComPASSION Team, The Royal Bournemouth and

Christchurch Hospital NHS Foundation Trust, Dorset HealthCare University NHS Foundation Trust.

•Person with diabetes (PWD) to scan Libre before each meal.•Insulin administered by staff. Stage 1

• PWD to scan Libre before each meal.• Staff dial up insulin dose. PWD administers insulin under staff supervision.

Stage 2a

• PWD to scan Libre before each meal.• PWD dials up insulin dose. PWD administers insulin under staff supervision.

Stage 2b

• PWD to scan Libre before each meal and dials up insulin dose.• Insulin administered by PWD with staff support as required.Stage 3

• PWD to scan Libre before each meal and dials up insulin dose.• Insulin administered independently by the PWD.Stage 4

Patient details:

Date of care plan:


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3. Current doses Long-acting insulin Rapid-acting insulin No. of Units No. of Units: Breakfast Lunch Evening meal Snacks

• Carbohydrate ratios when appropriate 1 unit of insulin for every ……… grams carbohydrate breakfast

……… grams carbohydrate lunch

……… grams carbohydrate evening meal

• Adjustment doses

1 unit of insulin will reduce blood sugar by Units 4. Insulin refusal

• Encourage insulin pre-meal as per prescription chart.

• Fixed doses basal and bolus meals only (no snacks) no dose adjustments + sick day rules (see Ketone Management Plan)Stage 1

• Boluses added for snacks + fixed basal + bolus dosing + sick day rules (see Ketone Management Plan)Stage 2

• Dose adjustments added to fixed doses bolus and basal + sick day rules (see Ketone Management Plan)Stage 3

• Introduce carbohydrate counting + dose adjustments + sick day rules (see Ketone Management Plan)Stage 4

Other

Specify: ......................................... Specify: .....................................


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• If not accepted within 5 minutes, continue with meal and offer again ONCE post meal.

• If insulin refused, follow Ketone Management Plan.

5. Carbohydrate refusal

• If a person refuses their meal or the carbohydrate part of their meal or a snack and have taken their rapid-acting insulin for that meal or snack, monitor their blood glucose levels every hour for the next four hours.

• If the person will accept carbohydrate in the interim this should be accommodated, e.g.: A milky drink with 2–3 biscuits, 2 slices of toast with spread and jam or the snack previously declined. Adjust accordingly for ½ portions or the person’s tolerance to accepting some carbohydrate.

• If the person’s blood glucose levels fall below 4 mmol/L treat as per the hypoglycaemia management plan.

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Abbreviations

BD bis die (twice daily)

BMI body mass index

CVD cardiovascular disease

DKA diabetic ketoacidosis

GLP-1 glucagon-like peptide 1

mBMI mean body mass index

PWD person with diabetes

RMN registered mental health nurse

SEDU specialist eating disorder unit

SGLT-2 sodium-glucose cotransporter-2

TDS ter die sumendum (three times daily)

T1DE type 1 diabetes and eating disorder

TREND-UK Training, Research and Education for Nurses in Diabetes-UK

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